Our long-term goal is to understand the functional organization of luteinizing homone-releasing hormone (LHRH) neurons which form the final common pathway of a neural pulse generator controlling the episodic secretion of pituitary gonadotropins. In the Suffolk ewe, environmental cues conveying daylength (photoperiod) and endogenous steroid hormones regulate the activity of the LHRH pulse generator, and are responsible for the phenomenon of seasonal breeding. Using immunocytochemistry, at a light and electron microscopic levels, we have recently found evidence of seasonal plasticity in the denisty of synaptic inputs onto LHRH neurons in the ewe. We now wish to extend these studies and address other issues concerning the LHRH neurosecretory system at cellular level. Critical to the interpretation of seasonal plasticity in the LHRH system is a knowledge of which LHRH cells project to the median eminence, and thereby constitute the pulse generator. Using a combination of retrograde tract tracing techniques and immunocytochemistry, we will determine which LHRH cells project to the median eminence, and whether they differ from LHRH cells which project elsewhere in either their location, innervation, or the neurochemical identity of their synaptic inputs. We will extend our present observations of seasonal plasticity in the synaptic inputs of LHRH neurons, and determine whether these changes are due to photoperiodic and/or steroid hormone signals. If photoperiod plays a major role in regulating the density of synaptic inputs onto LHRH neurons, we will determine whether these changes occur during photorefractoriness to a constant photoperiod, the key mechanisms by which photoperiod regulates seasonal breeding in the ewe. If photoperiod does not appear to contribute to the regulation of synaptic density onto LHRH cells, we will determine whether these alterations are due to maintained levels of estradiol and/or progesterone. Finally, we will investigate the potential neuroanatomical locus at which estradiol and progesterone influence the activity of the LHRH pulse generator by using a double label immunoeytochemical protocol to localize estradiol and progesterone receptors within LHRH neurons, or those catecholamine, GABA and beta-endorphin containing neurons which be afferent to them.